We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."

For more on the information mentioned here, see the following videos that take a closer look at these major topics:

We've known that being overweight and obese are important risk factors for type 2 diabetes, but, until recently, not much attention has been paid to the role of specific foods. I discuss this issue in my video, Why Is Meat a Risk Factor for Diabetes?

A 2013 meta-analysis of all the cohorts looking at the connection between meat and diabetes found a significantly higher risk associated with total meat consumption--especially consumption of processed meat, particularly poultry. But why? There's a whole list of potential culprits in meat: saturated fat, animal fat, trans fats naturally found in meat, cholesterol, or animal protein. It could be the heme iron found in meat, which can lead to free radicals and iron-induced oxidative stress that may lead to chronic inflammation and type 2 diabetes, or advanced glycation end (AGE) products, which promote oxidative stress and inflammation. Food analyses show that the highest levels of these so-called glycotoxins are found in meat--particularly roasted, fried, or broiled meat, though any foods from animal sources (and even high fat and protein plant foods such as nuts) exposed to high dry temperatures can be potent sources of these pro-oxidant chemicals.

In another study, researchers fed diabetics glycotoxin-packed foods, like chicken, fish, and eggs, and their inflammatory markers--tumor necrosis factor, C-reactive protein, and vascular adhesion molecules--shot up. "Thus, in diabetes, environmental (dietary) AGEs promote inflammatory mediators, leading to tissue injury." The good news is that restriction of these kinds of foods may suppress these inflammatory effects. Appropriate measures to limit AGE intake, such as eliminating meat or using only steaming and boiling as methods for cooking it, "may greatly reduce the already heavy burden of these toxins in the diabetic patient." These glycotoxins may be the missing link between the increased consumption of animal fat and meats and the development of type 2 diabetes.

Since the 2013 meta-analysis was published, another study came out in which approximately 17,000 people were followed for about a dozen years. Researchers found an 8% increased risk for every 50 grams of daily meat consumption. Just one quarter of a chicken breast's worth of meat for the entire day may significantly increase the risk of diabetes. Yes, we know there are many possible culprits: the glycotoxins or trans fat in meat, saturated fat, or the heme iron (which could actually promote the formation of carcinogens called nitrosamines, though they could also just be produced in the cooking process itself). However, we did learn something new: There also appears to be a greater incidence of diabetes among those who handle meat for a living. Maybe there are some diabetes-causing zoonotic infectious agents--such as viruses--present in fresh cuts of meat, including poultry.

A "crucial factor underlying the diabetes epidemic" may be the overstimulation of the aging enzyme TOR pathway by excess food consumption--but not by the consumption of just any food: Animal proteins not only stimulate the cancer-promoting hormone insulin growth factor-1 but also provide high amounts of leucine, which stimulates TOR activation and appears to contribute to the burning out of the insulin-producing beta cells in the pancreas, contributing to type 2 diabetes. So, it's not just the high fat and added sugars that are implicated; critical attention must be paid to the daily intake of animal proteins as well.

According to a study, "[i]n general, lower leucine levels are only reached by restriction of animal proteins." To reach the leucine intake provided by dairy or meat, we'd have to eat 9 pounds of cabbage or 100 apples to take an extreme example. That just exemplifies the extreme differences in leucine amounts provided by a more standard diet in comparison with a more plant-based diet.

I reviewed the role endocrine-disrupting industrial pollutants in the food supply may play in a three-part video series: Fish and Diabetes, Diabetes and Dioxins, and Pollutants in Salmon and Our Own Fat. Clearly, the standard America diet and lifestyle contribute to the epidemic of diabetes and obesity, but the contribution of these industrial pollutants can no longer be ignored. We now have experimental evidence that exposure to industrial toxins alone induces weight gain and insulin resistance, and, therefore, may be an underappreciated cause of obesity and diabetes. Consider what's happening to our infants: Obesity in a six-month-old is obviously not related to diet or lack of exercise. They're now exposed to hundreds of chemicals from their moms, straight through the umbilical cord, some of which may be obesogenic (that is, obesity-generating).

The millions of pounds of chemicals and heavy metals released every year into our environment should make us all stop and think about how we live and the choices we make every day in the foods we eat. A 2014 review of the evidence on pollutants and diabetes noted that we can be exposed through toxic spills, but "most of the human exposure nowadays is from the ingestion of contaminated food as a result of bioaccumulation up the food chain. The main source (around 95%) of [persistent pollutant] intake is through dietary intake of animal fats."

For more on the information mentioned here, see the following videos that take a closer look at these major topics:

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

Depression is a serious and common mental disorder responsible for the majority of suicides. As I've covered in Antioxidants & Depression, intake of fruits, vegetables, and naturally occurring antioxidants have been found to be protectively associated with depression. Therefore, researchers have considered that "it may be possible to prevent depression or to lessen its negative effects through dietary intervention."

But not so fast. Cross-sectional studies are snapshots in time, so we don't know "whether a poor dietary pattern precedes the development of depression or if depression causes poor dietary intake." Depression and even treatments for depression can affect appetite and dietary intake. Maybe people who feel crappier just eat crappier, instead of the other way around.

What we need is a prospective study (a study performed over time) where we start out with people who are not depressed and follow them for several years. In 2012, we got just such a study, which ran over six years. As you'll see in my video Fish Consumption and Suicide, those with higher carotenoid levels in their bloodstream, which is considered a good indicator of fruit and vegetable intake, had a 28% lower risk of becoming depressed within that time. The researchers conclude that having low blood levels of those healthy phytonutrients may predict the development of new depressive symptoms. What about suicide?

Worldwide, a million people kill themselves every year. Of all European countries, Greece appears to have the lowest rates of suicide. It may be the balmy weather, but it may also have something to do with their diet. Ten thousand people were followed for years, and those following a more Mediterranean diet pattern were less likely to be diagnosed with depression. What was it about the diet that was protective? It wasn't the red wine or fish; it was the fruit, nuts, beans, and effectively higher plant to animal fat ratio that appeared protective. Conversely, significant adverse trends were observed for dairy and meat consumption.

A similar protective dietary pattern was found in Japan. A high intake of vegetables, fruits, mushrooms, and soy products was associated with a decreased prevalence of depressive symptoms. The healthy dietary pattern was not characterized by a high intake of seafood. Similar results were found in a study of 100,000 Japanese men and women followed for up to 10 years. There was no evidence of a protective role of higher fish consumption or the long-chain omega 3s EPA and DHA against suicide. In fact, they found a significantly increasedrisk of suicide among male nondrinkers with high seafood omega 3 intake. This may have been by chance, but a similar result was found in the Mediterranean. High baseline fish consumption with an increase in consumption were associated with an increased risk of mental disorders.

One possible explanation could be the mercury content of fish. Could an accumulation of mercury compounds in the body increase the risk of depression? We know that mercury in fish can cause neurological damage, associated with increased risk of Alzheimer's disease, memory loss, and autism, but also depression. Therefore, "the increased risk of suicide among persons with a high fish intake might also be attributable to the harmful effects of mercury in fish."

Large Harvard University cohort studies found similar results. Hundreds of thousands were followed for up to 20 years, and no evidence was found that taking fish oil or eating fish lowered risk of suicide. There was even a trend towards higher suicide mortality.

What about fish consumption for the treatment of depression? When we put together all the trials done to date, neither the EPA nor DHA long-chain omega-3s appears more effective than sugar pills. We used to think omega-3 supplementation was useful, but several recent studies have tipped the balance the other way. It seems that "[n]early all of the treatment efficacy observed in the published literature may be attributable to publication bias," meaning the trials that showed no benefit tended not to get published at all. So, all doctors saw were a bunch of positive studies, but only because a bunch of the negative ones were buried.

What about antidepressant drugs? Sometimes they can be absolutely life-saving, but other times they may actually do more harm than good. See my controversial video Do Antidepressant Drugs Really Work?.

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

A study out of the University of North Carolina found no association between dietary fiber intake and diverticulosis. They compared those who ate the highest amount of fiber, 25 grams, to those who ate the smallest amount, which was three times lower at only 8 grams. Finding no difference in disease rates, researchers concluded that a low-fiber diet was not associated with diverticulosis.

The university sent out a press release entitled: "Diets high in fiber won't protect against diverticulosis." The media picked it up and ran headlines such as "High-fiber diet may not protect against diverticulosis, study finds." It went all over the paleo blogs and even medical journals, publishing such statements as an "important and provocative paper...calls into question" the fiber theory of the development of diverticulosis. Other editorials, though, caught the study's critical flaw. To understand this, let's turn to another dietary deficiency disease: scurvy.

Medical experiments on prisoners at Iowa State Penitentiary showed that clinical signs of scurvy start appearing after just 29 days without vitamin C. Experiments on pacifists during World War II showed that it takes about 10 mg of vitamin C a day to prevent scurvy. Imagine going back a few centuries when they were still trying to figure scurvy out. Dr. James Linde had this radical theory that citrus fruits could cure scurvy. What if an experiment was designed to test this crazy theory, in which sailors were given the juice of either one wedge of lemon or three wedges of lemon each day? If a month later on the high seas there was no difference in scurvy rates, one might see headlines from printing presses touting that a low-vitamin C diet is not associated with scurvy.

Well, a wedge of lemon only yields about 2 mg of vitamin C, and it takes 10 mg to prevent scurvy. They would have been comparing one vitamin C-deficient dose to another vitamin C-deficient dose. No wonder there would be no difference in scurvy rates. We evolved eating so many plants that we likely averaged around 600 mg of vitamin C a day. That's what our bodies are biologically used to getting.

What about fiber? How much fiber are we used to getting? More than 100 grams a day! The highest fiber intake group in the North Carolina study was only eating 25 grams, which is less than the minimum recommended daily allowance of about 32 grams. The subjects didn't even make the minimum! The study compared one fiber-deficient diet to another fiber-deficient diet--no wonder there was no difference in diverticulosis rates.

The African populations with essentially no diverticulosis ate diets consisting in part of very large platefuls of leafy vegetables--similar, perhaps, to what we were eating a few million years ago. They were eating plant-based diets containing 70 to 90 grams of fiber a day. Most vegetarians don't even eat that many whole plant foods, although some do. At least vegetarians tend to hit the minimum mark, and they have less diverticulosis to show for it. A study of 47,000 people confirmed that "[c]onsuming a vegetarian diet and a high intake of dietary fiber were both associated with a lower risk of admission to hospital or death from diverticular disease." They had enough people to tease it out. As you'll see in my video Does Fiber Really Prevent Diverticulosis?, compared to people eating a single serving of meat a day or more, those who ate less than half a serving appeared to have a 16% lower risk and pescatarians (eating no meat except fish) had a risk down around 23%. Both of these results weren't in and of themselves statistically significant, but eating vegetarian was. Vegetarians had 35% lower risk, and those eating strictly plant-based appeared to be at 78% lower risk.

As with all lifestyle interventions, it only works if you do it. High-fiber diets only work if they're actually high in fiber.

People commonly ask Do Vegetarians Get Enough Protein?, but maybe they should be more concerned where everyone else is getting their fiber. Ninety-seven percent of Americans don't even reach the recommended daily minimum.

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."

The results of the CHAMACOS (Center for the Health Assessment of Mothers and Children of Salinas) study were published recently. This study of a California birth cohort investigated the relationship between exposure to flame retardant chemical pollutants in pregnancy and childhood, and subsequent neurobehavioral development. Why California? Because California children's exposures to these endocrine disruptors and neurotoxins are among the highest in the world.

What did they find? The researchers concluded that both prenatal and childhood exposures to these chemicals "were associated with poorer attention, fine motor coordination, and cognition" (particularly verbal comprehension) by the time the children reached school age. "This study, the largest to date, contributes to growing evidence suggesting that PBDEs [polybrominated diphenyl ethers, flame retardant chemicals] have adverse impacts on child neurobehavioral development." The effects may extend into adolescence, again affecting motor function as well as thyroid gland function. The effect on our thyroid glands may even extend into adulthood.

These chemicals get into moms, then into the amniotic fluid, and then into the breast milk. The more that's in the milk, the worse the infants' mental development may be. Breast milk is still best, but how did these women get exposed in the first place?

The question has been: Are we exposed mostly from diet or dust? Researchers in Boston collected breast milk samples from 46 first-time moms, vacuumed up samples of dust from their homes, and questioned them about their diets. The researchers found that both were likely to blame. Diet-wise, a number of animal products were implicated. This is consistent with what's been found worldwide. For example, in Europe, these flame retardant chemical pollutants are found mostly in meat, including fish, and other animal products. It's similar to what we see with dioxins--they are mostly found in fish and other fatty foods, with a plant-based diet offering the lowest exposure.

If that's the case, do vegetarians have lower levels of flame retardant chemical pollutants circulating in their bloodstreams? Yes. Vegetarians may have about 25% lower levels. Poultry appears to be the largest contributor of PBDEs. USDA researchers compared the levels in different meats, and the highest levels of these pollutants were found in chicken and turkey, with less in pork and even less in beef. California poultry had the highest, consistent with strict furniture flammability codes. But it's not like chickens are pecking at the sofa. Chickens and turkeys may be exposed indirectly through the application of sewer sludge to fields where feed crops are raised, contamination of water supplies, the use of flame-retarded materials in poultry housing, or the inadvertent incorporation of fire-retardant material into the birds' bedding or feed ingredients.

Fish have been shown to have the highest levels overall, but Americans don't eat a lot of fish so they don't contribute as much to the total body burden in the United States. Researchers have compared the level of PBDEs found in meat-eaters and vegetarians. The amount found in the bloodstream of vegetarians is noticeably lower, as you can see in my video Flame Retardant Pollutants and Child Development. Just to give you a sense of the contribution of chicken, higher than average poultry eaters have higher levels than omnivores as a whole, and lower than average poultry eaters have levels lower than omnivores.

What are the PBDE levels in vegans? We know the intake of many other classes of pollutants is almost exclusively from the ingestion of animal fats in the diet. What if we take them all out of the diet? It works for dioxins. Vegan dioxin levels appear markedly lower than the general population. What about for the flame retardant chemicals? Vegans have levels lower than vegetarians, with those who've been vegan around 20 years having even lower concentrations. This tendency for chemical levels to decline the longer one eats plant-based suggests that food of animal origin contributes substantially. But note that levels never get down to zero, so diet is not the only source.

The USDA researchers note that there are currently no regulatory limits on the amount of flame retardant chemical contamination in U.S. foods, "but reducing the levels of unnecessary, persistent, toxic compounds in our diet is certainly desirable."